1. Field of the Invention
The present invention relates generally to occluding the septum of the heart. More particularly, the present invention relates to magnetic devices and method which can be used to occlude holes or ruptures in the atrial and ventricular septa of the heart.
2. Background of the Invention
There are many congenital defects that may be present in human beings. Of such defects, atrial septal defects (ASDs) are congenital abnormalities characterized by an alteration in the structure of the atrial septum. The frequency of these abnormalities is about 10% of all congenital heart disease, with a 3:2 female/male ratio.
The physiological outcome of an atrial septal defect is influenced by the size of the ASD and duration of the shunt, and on the reaction of the pulmonary vascular bed. In large ASDs with significant left-to-right shunts, the defect produces an important volume-overloaded in the right atrium and right ventricle, with an increased volume ejected into a low-resistance pulmonary vascular bed. This may result in the development in adulthood of pulmonary vascular occlusive disease and pulmonary arterial hypertension. The rate of survival in young adults when they develop progressive pulmonary hypertension is limited.
Patients diagnosed as having secundum ASDs with a significant shunt (defined as a pulmonary blood flow to systemic blood flow ratio (Qp/Qs) of >1.5) are operated upon ideally before 5 years of age or whenever a diagnosis is made in later years. In the past, cardiac catheterization oximetry measurement was performed to evaluate the magnitude of left-to-right shunt. Currently, two-dimensional echocardiography and Doppler color flow mapping is typically used to visualize the anatomy of the defect and estimate the Qp/Qs ratio from Doppler indices.
ASDs are classified by size: small defects with a maximal diameter >3 mm to <6 mm, moderate defects measured ≥6 mm to <12 mm and large defects were ≥12 mm. Two thirds of the ASDs secundum type may increase as time goes by. This makes them candidates for transcatheter closure with specific devices. ASD is the second most common congenital heart lesion in adult and children as well.
Transcatheter closures for atrial septal defects were performed for the first time in experimental animal models and humans by King and Mills. Some researchers developed a single disk-device with tethering hooks but the implantation was difficult. The two devices currently undergoing evaluation, the Lock “clamshell” device and the Sideris “buttoned” device are essentially umbrella-like devices for supporting the fabric patches. Problems with the clamshell device include spontaneous device embolization, persistent residual shunts in as many as 26% of patients and wire fractures in up to 33% of patients on follow-up. Nowadays, Amplatzer symmetric and an asymmetric mechanical occluder are under current medical use.
A patent foramen ovale (PFO) is a persistent defect, usually a flap-like opening between the atrial septum primum and secundum at the location of the fossa ovalis. The foramen ovale is utilized during intrauterine life as a physiologic conduit for right-to-left blood shunting. Functional closure of the foramen ovale occurs after birth, once the pulmonary circulation has been established increasing left atrial blood flow and pressure. The persistence of patent foramen ovale has been found between 25-35% of adults in an autopsy series without a gender preference. Echocardiography is a method through which PFO can be detected in vivo in 5-20% in the adult population.
One of the major complications of PFO could be paradoxical embolism which is thought to be responsible for an embolic event in the absence of a left-sided thromboembolic source, the potential for right-to-left shunting, and the detection of thrombus in the venous system or right atrium.
The diagnosis of paradoxical embolism is usually presumptive. Its mechanisms are believed to be caused by: a chronic elevation of right atrial pressure with consecutive right-to-left shunt (e.g., pulmonary hypertension, COPD, pulmonary embolism), or a transient elevation of right atrial pressure after release of positive airway pressure (Valsalva, cough, diving).
A retrospective French multicenter study reported a yearly risk of 1.2% to sustain a recurrent TIA, and of 3.4% to suffer a recurrent stroke or TIA; this was despite medical treatment with oral anticoagulants or antiplatelet drugs in patients with PFO and cryptogenic stroke.
Nonsurgical closure of PFOs has become possible with the advent of transcatheter closure devices, initially developed for percutaneous closure of atrial septal defects (ASD).
Ventricular septal defect (VSD) is the most common congenital heart disease (approximately 20%). The perimembranous (PmVSD) defect, involving the membranous septum and the adjacent area of muscular septum is presented in about 70% of all VSD. Surgical repair is the most common treatment with low postoperative mortality but still with potential risks of complete heart block, chylothorax, phrenic nerve injury, early and late arrhythmias, postpericardiotomy syndrome, wound infection, and neurologic sequelae of cardiopulmonary bypass.
The failure of different devices to occlude the VSD were related to large delivery sheaths (11-F) required, complex implantation techniques, inability to reposition and redeploy the device, and mainly interference with the aortic and tricuspid valves and significant residual shunts (25% to 60%). The criteria to include the closure of PmVSD include, but are not limited to: echocardiographic studies, symptoms of heart failure or evidence of left atrial and or left ventricular enlargement.
The Amplatzer Membranous VSD Occluder is the only device currently used specifically designed for PmVSDs occlusion. However, this device typically cannot be used if: 1) body weight <8 kg, 2) subaortic rim as shown by echocardiography in the long-axis view <2 mm, 3) left ventricle to right atrial shunting, 4) right to left shunting through the defect, 5) PmVSD with an aneurysm and multiple shunts that could not be successfully closed with one device, 6) sepsis, 7) complex heart lesions such as tetralogy of Fallot, 8) contraindication to antiplatelet therapy.
During myocardial infarction, ventricular septal rupture can occur. Ventricular septal rupture is one of at least three mechanical complications that can occur following myocardial infarction. The septal rupture can result from full thickness infarction of the interventricular septum followed by enough necrosis to result in the septal rupture. Others myocardial infarction complications are free wall rupture, and papillary muscle rupture. Free wall rupture usually results in rapid death while papillary muscle rupture results in sudden mitral regurgitation.
At present with thrombolysis treatment in acute myocardial infarction and early intervention, the incidence of postinfarction ventricular septal rupture has diminished from the 1-3% to 0.2%. The risk factors associated with this severe complication (IVSR) include advanced age, anterior infarction, female gender and smoking history and lack of collateral circulation.
The post AMI ventricular septal rupture can be divided into simple and complex. In the former, the rupture connects the two ventricles without gross hemorrhage or muscle laceration and with the opening between right and left ventricle at the same horizontal level of the ventricular septum. This is more frequent in the anterior infarct. In the latter, the interventricular communication presents a convoluted course with a tract that might extend into regions remote from the primary AMI site. This rupture is more complex due to the presence of hemorrhage, disruption of myocardial muscle and multiple perforations. This often occurs in multiple vessel disease and inferior myocardial infarction.
In a GUSTO-I (global utilization of streptokinase and t-PA for occluded coronary arteries) trial there was an incidence of 0.2% of ventricular septal rupture in over 41,000 patients, a 5-10 fold reduction as compared with the pre-thrombolytic era. Nowadays, the average time interval between infarction and rupture is nearly one day, while before the thrombolytic area it was between 5-6 days. However, the surgical mortality ultimately has increased maybe due to the change in the patient population. At present, the thrombolytic treatment may augment the complex rupture portion which is more difficult to repair surgically, instead of the simple ruptures. Moreover, patients in the first 24-48 hours after infarction are less likely to sustain the surgical trauma than they would be a week or so later.
The post-myocardial septal rupture consequence is the shunting of oxygenated blood from the left to the right ventricle. The right ventricle, generally involved in the infarct, suffers an augmented volume load. The factors that are related with poor outcome are hypotension, oliguria, elevated creatinine, and cardiogenic shock to be associated with non-survivors. A multivariate analysis demonstrated that increasing age, anterior infarction, and female sex as predictors of ventricular septal rupture. When the right ventricular is involved in the infarction the outcome is generally poor—only about 24% with poor right ventricular free wall contraction survived compared to about 80% survival with a good right ventricular function.
The GUSTO-I study trial showed that patients treated surgically had a 47% mortality rate within a 30 day period while for non surgical patients mortality rate was 94%. In the SHOCK trial the hospital patients with cardiogenic shock who underwent surgical repair of ventricular septal rupture mortality was 81%.
The surgical principles for occlusion of VSR include hypothermia during cardiopulmonary bypass with myocardial protection, trans-infarction approach to the VSR, trimming of infarcted muscle around the VSR, closure of the VSR with a patch to avoid tension, closure of the ventricle without tension with buttressed sutures.
In spite of these surgical measurements, the residual or recurrent ventricular septal defect following initial surgical repair was as high as 20% of the cases due to the infarct extension leading to patch dehiscence or creation of a new VSD.
Another option is transcatheter closure of VSR, which is exigent because the patients are seriously ill. Moreover, patients referred for transcatheter closure have generally been rejected for surgical closure due to cardiogenic shock or advanced age.
So far, ventricular septal rupture repair continues to be a challenge. There have only been a few single case reports and small series. Others reported successful closure, using an Amplatzer septal occluder, of a residual defect following surgical patch closure.
Others have suggested that device closure may provide temporary stabilization of the haemodynamic alteration. This may allow surgical closure after the infarcted myocardium around the rupture has had time to fibrose. With the current devices, closure is most difficult while the margins of the rupture are soft and necrotic.